Neurosurg Focus 16 (6):e4, 2004, Click here to return to Table of Contents

Conus medullaris and cauda equina syndrome

as a result of traumatic injuries: management principles

JAMES S. HARROP, M.D., GABRIEL E. HUNT JR., M.D., AND ALEXANDER R. VACCARO, M.D.
Department of Neurosurgery, and Department of Orthopaedics, Jefferson Medical College,
Rothman Institute, Philadelphia, Pennsylvania

Conus medullaris syndrome (CMS) and cauda equina syndrome (CES) are complex neurological disorders that can
be manifested through a variety of symptoms. Patients may present with back pain, unilateral or bilateral leg pain,
paresthesias and weakness, perineum or saddle anesthesia, and rectal and/or urinary incontinence or dysfunction.
Although patients typically present with acute disc herniations, traumatic injuries at the thoracolumbar junction at the
terminal portion of the spinal cord and cauda equina are also common. Unfortunately, a precise understanding of the
pathophysiology and optimal treatments, including the best timing of surgery, has yet to be elucidated for either trau-
matic CES or CMS. In this paper the authors review the current literature on traumatic conus medullaris and cauda
equina injuries and available treatment options.

KEY WORDS • cauda equina syndrome • conus medullaris syndrome • trauma

Conus medullaris syndrome and CES are complex neu-
rological disorders manifesting a myriad of symptoms
such as back pain, unilateral or bilateral leg pain, pares-
thesias and weakness, perineum or saddle anesthesia, and
rectal and/or urinary incontinence or dysfunction. Patients
with CES typically present with symptoms of lumbosacral
radiculopathies, whereas those with CMS present with
symptoms consistent with spinal cord compression and
dysfunction. Both syndromes may occur following trau-
matic injury to the thoracolumbar junction or the lum-
bosacral regions.
In a report on intervertebral disc herniation, Mixter and
Barr33 initially described the relationship between CES
and lumbosacral nerve compression as a result of disc her-
niation. Although CES is clearly related to the presence of
an acute large lumbosacral disc herniation, its relationship
to acute traumatic injury to the thoracolumbar junction is
less clearly defined. Many authors2,3,14,17,18,22,27,34,36,40,41 have
defined variable treatment algorithms for the management
of CES caused by acute herniation of the nucleus pul-
posus. Nonetheless, a precise understanding of the patho-
physiology and optimal treatments, including the timing
of the latter, has yet to be elucidated for either traumatic
CES or CMS.
ANATOMY, DISEASE, AND IMAGING
Anatomical Considerations
In neonates, the spinal cord terminates at the end of the
vertebral column or the lumbosacral junction. Note, how-
Abbreviations used in this paper: CES = cauda equina syndrome;
CMS = conus medullaris syndrome; CT = computerized tomogra-
phy; MR = magnetic resonance.
ever, that the location of the terminal end of the spinal
cord, or the conus medullaris, varies as the infant devel-
ops.29 During infancy the spinal cord terminates between
the first and third lumbar vertebrae, whereas in adults it is
positioned between the 12th thoracic and the second lum-
bar vertebrae. In a detailed anatomical review of the conus
medullaris in the adult human, Malas and colleagues29
found that the conus had a variable location between T-12
and L-2.
The thoracolumbar region is where the rigid thoracic
kyphosis transitions into the mobile lumbar lordosis and is
therefore susceptible to traumatic injuries.35 This transi-
tion generally occurs at T11–12, although in elderly pa-
tients with osteopenia the transition point generally
migrates caudally due to the increased degree of thoracic
kyphosis in this population.4,14,39 In the vicinity of the tho-
racolumbar junction in an adult, the spinal cord terminates
as the conus medullaris. Anatomically, this is a dilation of
the distal portion of the spinal cord and is the site of tran-
sition from the central to peripheral nervous system (cau-
da equina). This is a very important distinction given the
implications for recovery following injury. Patients with
an injury above the conus medullaris typically present
with symptoms consistent with spinal cord injury, where-
as those with injuries below this level may present with
symptoms consistent with lumbosacral radiculopathies.
Lesions affecting the transition between the two regions
can cause symptoms consistent with both upper and lower
motor neuron dysfunction.
Natural History of Injury to the Conus Medullaris or
Cauda Equina
Neurological recovery from injury to the conus med-
ullaris or cauda equina is variable and unpredictable and

Neurosurg. Focus / Volume 16 / June, 2004 19

 J. S. Harrop, et al.

may be influenced by many unrelated factors such as

patient age, vascular supply to the region, energy transfer
to neural elements, pharmacological means to modify the
secondary cascade of injury, and timing of neural decom-
pression. Traumatic lesions of the cauda equina, which
cause sudden, acute neurological deterioration as opposed
to the gradual onset of lower motor neuron dysfunction in
chronic CES, generally have a poorer prognosis.27
Patient Assessment
In a minority of patients with a clinically unstable trau-
ma, fractures are not identified immediately during the re-
suscitative period. It has been reported that between 5 and
15% of patients with multisystem trauma often have an
occult fracture that is not diagnosed during their initial
evaluation.9,15,23,28 This is particularly pertinent in the con-
text of an unrecognized cauda equina or conus medullaris
injury given the potential for a more optimal return of neu-
rological function through directed nonsurgical or surgical
intervention.1,27 Additionally, symptoms of CES or CMS
may be extremely subtle and therefore a heightened de-
gree of suspicion is necessary when encountering trau-
matic lesions of the thoracolumbar junction so as not to Fig. 1. Lateral (left) and anteroposterior (right) plain radio-
miss an accurate diagnosis. At times, results of the neuro- graphs of the thoracolumbar spine obtained following an L-1 flex-
ion compression injury.
logical examination may only reveal the presence of mild
unilateral perineal anesthesia or urinary retention, findings
often missed on routine placement of indwelling catheters
during the posttrauma resuscitation portion of a patient’s process due to the confined imaging space, and patients
workup. If an unstable fracture is not appropriately immo- with specific ferromagnetic implants cannot undergo MR
bilized, effects due to repeated trauma to the neural ele- imaging because of the risk of severe soft-tissue injury
ments may lead to further injury resulting in progressive due to foreign body migration. Findings on MR imaging
loss of motor and bowel/bladder function. have been correlated with neurological recovery follow-
ing trauma; that is, the presence of hemorrhage within the
Spinal Imaging spinal cord parenchyma is associated with minimal neuro-
logical recovery.37
Plain radiographs of the entire spinal axis provide the Note that MR imaging studies are especially useful in
medical team with an immediate understanding of spinal
alignment and the presence of any obvious traumatic dis-
ruption of the osteoligamentous anatomy of the vertebral
column (Fig. 1). Results positive for trauma on radiogra-
phy and neurological examination lead to a more focused
investigation by using advanced imaging modalities.
Computerized tomography scanning provides optimal as-
sessment of bone anatomy and the degree of canal occlu-
sion due to retropulsed bone fragments in the setting of a
burst fracture (Fig. 2).12,13 Nonetheless, CT scanning has a
limited capacity for visualizing the precise size of a trau-
matic disc herniation, the presence of epidural or subdu-
ral hematomas, the nature and degree of ligamentous dis-
ruption, or the changes in spinal cord parenchyma.16
Magnetic resonance imaging has further improved our
ability to visualize and comprehend the degree of soft-tis-
sue ligamentous injury, intravertebral disc disruption and
herniation, spinal cord parenchymal edema, and hemor-
rhage or disruption following spinal injury (Figs. 3 and 4).
Magnetic resonance imaging is a noninvasive, nonioniz-
ing modality that allows improved visualization of the
spinal cord parenchyma and adjacent soft-tissue struc-
tures.25 Unfortunately, this method is not without its draw-
backs: it may not always be available in all institutions at Fig. 2. Sagittal reconstructed (left) and axial (right) CT scans of
all times, it requires more time to obtain a full complement the thoracolumbar spine demonstrating an L-4 burst fracture with
of images compared with the time taken using other imag- retropulsion of bone into the spinal canal (arrows) and compres-
ing modalities, some patients are uncomfortable with the sion of the distal lumbar and sacral nerve rootlets.

20 Neurosurg. Focus / Volume 16 / June, 2004

Treatment of spinal syndromes resulting from traumatic injury
Fig. 3. Magnetic resonance image of the thoracolumbar spine
revealing an L-4 burst fracture with retropulsion of bone into the
spinal canal (arrow) and compression of the distal lumbar and
sacral nerve rootlets.
demonstrating the thoracolumbar junction due to the vari-
able location of the conus medullaris at this level in the
adult population.29 Patients with neurological dysfunction
referable to this region can be difficult precisely to classi-
fy neurologically due to the possibility of injury to both
the cauda equina and the conus medullaris; the presence of
lumbar spinal nerve root sparing and delayed reflex recov-
ery, especially in the setting of drug-induced sedation; and
Fig. 4. A T2-weighted MR image of the thoracolumbar spine
demonstrating an L-1 burst fracture with retropulsion of bone into
the spinal canal (arrow) and compression of the spinal cord (conus
medullaris). Note the increased signal representing cord edema.
Neurosurg. Focus / Volume 16 / June, 2004
the presence of an indwelling catheter. Accurate neural
visualization may help to clarify the pathophysiology in
this clinical situation.
DISEASE MANAGEMENT PRINCIPLES
The thoracolumbar junction is a spinal region vulnera-
ble to traumatic injury. Mechanisms may include blunt
trauma from motor vehicle collisions or penetrating in-
juries from gunshot or knife injuries. A majority of in-
juries occurring at this level are either compression or
burst fractures. The former type are usually not associated
with any neurological deficit given that there is no viola-
tion of the spinal canal due to spinal misalignment or
retropulsed bone fragments.
Burst fractures by definition involve compromise of the
spinal canal by the middle spinal column or spinal mis-
alignment (Fig. 4). These fractures are often managed
nonsurgically unless there is significant disruption of the
posterior osteoligamentous complex with kyphotic defor-
mity or the presence of a neurological deficit in the setting
of significant thecal sac compression. Fractures at the
level of the conus medullaris and the cauda equina often
are associated with incomplete neurological deficits due
to the space available to the spinal cord at these levels.
Penetrating Injuries
Very few studies have been conducted on the treatment
of penetrating traumatic injuries to the cauda equina and
conus medullaris. In 1999 Flores, et al.,17 retrospectively
evaluated the neurological outcomes in 45 patients who
had incurred gunshot wounds to the spine. Sixty percent
of the patients presented with symptoms consistent with
CES. Following laminectomy, 53% of these patients dem-
onstrated improvement in their symptoms. Only a handful
of case reports have been published on the onset of CES
following stab wounds, the administration of epidural
anesthesia, and the spontaneous occurrence of epidural
and subdural hematomas from anticoagulation thera-
py.17,40,41 The unifying theme in all of these publications
has been the concept of timely diagnosis and surgical de-
compression in the context of obvious thecal sac com-
pression. Unfortunately, even with timely surgical inter-
vention in these scenarios, functional outcome has often
been unpredictable.
Blunt Trauma
Presently, there is significant controversy concerning
the appropriate treatment algorithm in patients who sus-
tain a traumatic injury to either the conus medullaris or
cauda equina following blunt trauma. The need for surg-
ery as well as its timing is often a conjectural matter with-
out the definitive support of Class I or II evidence-based
literature. No definitive treatment algorithm has been uni-
versally accepted for injuries to the conus medullaris or
cauda equina despite the number of retrospective reviews
on the subject matter. The goal of treatment in such sce-
narios is to attempt to maximize neurological recovery
while preventing further neurological decline and associ-
ated pain syndromes.
Once an injury to the conus medullaris or cauda equina
has been identified, early intervention is paramount. This
21

includes appropriate immobilization of the spinal column
and maintenance of physiological vital signs, especially
blood pressure and oxygenation. Intravenous administra-
tion of methylprednisolone has been advocated by re-
searchers in the National Acute Spinal Cord Injury Study
II and III studies in adult patients within 8 hours of spinal
cord injury. The effectiveness of this pharmacological reg-
imen has not been uniformly accepted, however.21 The
efficacy of steroid agents in modifying the secondary cas-
cade of injury to the peripheral nervous system, specifi-
cally in CES, has yet to be proven. Gok, et al.,20 examined
the efficacy of methylprednisolone in acute experimental
cauda equina injury in a rabbit model. They concluded
that both neurophysiological and histopathological study
results demonstrated the neuroprotective effectiveness of
methylprednisolone if the agent was administered within
8 hours of trauma.
Following hemodynamic stabilization, immobilization,
and the decision to administer selected pharmacological
agents, the treating physician must decide whether surgi-
cal intervention is necessary given the degree of fracture
stability. An unstable lesion is fraught with the potential
for progressive deformity and pain that may worsen the
presenting neurological status in the patient. Surgical in-
tervention is accepted in the setting of significant defor-
mity, that is, kyphosis, or in the presence of a progressive
neurological deficit in the setting of a spinal deformity or
static neurological compression.
A neurological deficit is present in approximately 4 to
42% of patients with thoracolumbar junction fractures.18
Many researchers believe that neurological damage pri-
marily occurs at the moment of maximal canal occlusion,
that is, at the time of injury, and that in the setting of a
complete spinal cord lesion, regardless of the degree of
residual canal occlusion, surgical decompression rarely, if
ever, enhances neurological recovery.5 In the event of an
incomplete neurological injury with persistent thecal com-
pression, many investigators advocate timely surgical de-
compression to maximize the potential for neurological
recovery of a conus medullaris or cauda equina injury.10
Boerger and colleagues5 performed a metaanalysis of the
world’s literature in 2000 to evaluate the effectiveness of
surgical decompression in the context of a neurological
deficit associated with a thoracolumbar burst fracture.
They found that patients with an incomplete neurological
deficit who had undergone surgical decompression and
stabilization experienced a better neurological recovery
compared with that in patients who had undergone non-
surgical treatment.5,7,8,24 Surgical intervention also de-
creased pain, reduced periods of postural reduction or
bedrest, and improved sagittal alignment to a greater de-
gree than nonsurgical intervention.19 At present, surgical
decompression in patients with a complete neurological
injury has not demonstrated any real benefit in terms
of overall neurological improvement.6 Surgery in this
context is intended to maximize rehabilitation potential,
shorten in-hospital and rehabilitation time, improve spinal
stability, and prevent future spinal deformity.
An anterior or posterolateral extracavitary approach
may allow for the effective decompression of neural ele-
ments in spinal cord compression. The anterior approach
is particularly useful in decompressing midline ventral le-
22
J. S. Harrop, et al.
sions and correcting severe kyphotic deformities.6,7 Bohl-
man6 reported superior neurological outcomes following
an anterior as opposed to a posterior decompressive pro-
cedure in patients with an incomplete thoracic spinal cord
injury. The major limitation of an anterior exposure is the
potential surgical violation of the pleural and/or peritoneal
cavities. McCormick30 reported the effective use of an an-
terior extrapleural technique in exposing the thoracic and
thoracolumbar spine and avoiding violation of the pleural
cavity.
Posterior decompression through a laminectomy fol-
lowing thoracic and thoracolumbar injuries has been
shown to be ineffective and should not be performed as an
isolated treatment strategy.6,34 Surgical removal of the pos-
terior osteoligamentous complex without a concomitant
fusion may allow for temporary neurological recovery.
Nonetheless, the vertebral column will be unable to main-
tain its alignment with the loss of its dorsal tension band,
and instability together with the potential for loss of spinal
alignment may ensue. The immediate result of removing
the dorsal osseous components is migration of the spinal
cord posteriorly if the spine has a lordotic alignment.
Note, however, that normal spinal alignment at the thora-
columbar junction is neutral to slightly kyphotic, which
does not allow for optimal thecal sac migration from an-
teriorly located retropulsed bone fragments. This may re-
sult in further neurological compromise due to tethering of
the neural elements (bowstring effect) over anterior bone
elements.
Advantages of the posterior approach lie in the fact that
it provides excellent visualization and access to the dorsal
thecal sac. These are useful in managing certain fracture
types because the reported incidence of thecal sac lacera-
tions together with possible nerve root incarceration after
traumatic thoracic and thoracolumbar burst fractures is
between 7 and 16%.26,38 An anterior approach will not
provide access to an entrapped lumbar nerve root in this
clinical situation.31 The presence of a central split in the
spinous process or greenstick fracture of the lamina on
preoperative transaxial CT studies may be an indicator of
a dural laceration, depending on its size and neural dis-
placement during force impact.32
The value of timely surgical intervention in a patient
with conus medullaris or cauda equina injury following
trauma is unclear at this time. Acute surgical intervention
in the first 24 to 48 hours after injury, especially by using
an anterior approach, is often associated with excessive
surgical bleeding, which has motivated many personnel to
delay surgical intervention for at least 2 to 3 days follow-
ing injury. The attempt to maximize neurological recovery
through immediate surgical decompression and stabiliza-
tion has not resulted in clinically improved neurological
outcomes compared with outcome following delayed sur-
gical intervention or nonsurgical treatment. In degener-
ative disease, surgical intervention within 48 hours of
symptoms of cauda equina dysfunction has been shown to
improve sensory, motor, urinary, and rectal abnormalities
significantly compared with intervention after more than
48 hours.3 Lesions involving the conus medullaris have a
less predictable response to immediate surgical interven-
tion.11 Patients with unilateral saddle dysethesias in the
setting of CES have a better prognosis for return of blad-
Neurosurg. Focus / Volume 16 / June, 2004
Treatment of spinal syndromes resulting from traumatic injury
der function compared with that in patients with bilateral
saddle anesthesia.27
In summary, the data available to prognosticate the re-
covery of neurological dysfunction following traumatic
conus medullaris or cauda equina injury is derived from
retrospective data regarding degenerative disease. Ob-
viously, this is far from satisfactory. Today the majority of
center personnel who frequently manage traumatic spinal
injuries recommend surgical intervention when the patient
is medically stable, that is, within the first 3 days of injury,
predictably to improve neurological recovery of an in-
complete spinal cord or cauda equina injury. More timely
intervention is reserved in the event of a progressive neu-
rological deficit with significant thecal sac compression.
References
1. Ahn UM, Ahn NU, Buchowski JM, et al: Cauda equine
syndrome secondary to lumbar disc herniation. Spine 25:
1515–1522, 2000
2. Beaunoyer M, St-Vil D, Lallier M, et al: Abdominal injuries
associated with thoraco-lumbar fractures after motor vehicle
collision. J Pediatr Surg 36:760–762, 2001
3. Bedbrook GM: Stability of spinal fractures and fracture dislo-
cations. Paraplegia 9:23–32, 1971
4. Besemann EF (ed): The Human Spine in Health and Disease,
by Georg Schmorl, ed 2. New York: Grune & Stratton, 1971,
pp 290–291
5. Boerger TO, Limb D, Dickson RA: Does ‘canal clearance’
affect neurological outcome after thoracolumbar burst frac-
tures? J Bone Joint Surg Br 82:629–635, 2000
6. Bohlman HH: Traumatic fractures of the upper thoracic spine
with paralysis. J Bone Joint Surg Am 56:1299, 1974 (Ab-
stract)
7. Bohlman HH, Freehafer A, Dejak J: The results of treatment of
acute injuries of the upper thoracic spine with paralysis. J Bone
Joint Surg Am 67:360–369, 1985
8. Bradford DS, Akbarnia BA, Winter RB, et al: Surgical stabi-
lization of fracture and fracture dislocations of the thoracic
spine. Spine 2:185–196, 1977
9. Chan RN, Ainscow D, Sikorski JM: Diagnostic failures in the
multiple injured. J Trauma 20:684–687, 1980
10. Chapman JR, Anderson PA: Thoracolumbar spine fractures and
neurologic deficits. Orthop Clin North Am 25:595–612, 1994
11. Chuang TY, Cheng H, Chan RC, et al: Neurourologic findings
in patients with traumatic thoracolumbar vertebra junction le-
sions. Arch Phys Med Rehabil 82:375–379, 2001
12. Dai LY: Remodeling of the spinal canal after thoracolumbar
burst fractures. Clin Ortho 382:119–123, 2001
13. de Klerk LW, Fontijne WP, Stijnen T, et al: Spontaneous re-
modeling of the spinal canal after conservative management of
thoracolumbar burst fractures. Spine 23:1057–1060, 1998
14. Dryden DM, Saunders LD, Rowe BH, et al: The epidemiology
of traumatic spinal cord injury in Alberta, Canada. Can J Neu-
rol Sci 30:113–121, 2003
15. Enderson BL, Reath DB, Meadows J, et al: The tertiary trauma
survey: a prospective study of missed injury. J Trauma 30:
666–670, 1990
16. Flanders AE: Thoracolumbar trauma imaging overview. Instr
Course Lect 48:429–431, 1999
17. Flores LP, Nascimento Filho Jde S, Periera Neto A, et al:
[Prognostic factors related to gunshot wounds to the spine in
patients submitted to laminectomy.] Arq Neuropsiquiatr 57:
836–842, 1999 (Por)
18. Gertzbein SD: Fractures of the Thoracic and Lumbar Spine.
Baltimore: Williams & Wilkins, 1992
19. Gertzbein SD: Scoliosis Research Society. Multicenter spine
fracture study. Spine 17:528–540, 1992
20. Gok A, Uk C, Yilmaz M, et al: Efficacy of methylprednisolone
Neurosurg. Focus / Volume 16 / June, 2004
in acute experimental cauda equina injury. Acta Neurochir
144:817–821, 2002
21. Hadley MN, Walters BL, Grabb PA, et al: Pharmacological
therapy after acute cervical spinal cord injury. Neurosurgery
50 (Suppl):S63–S71, 2002
22. Hu R, Mustard CA, Burns C: Epidemiology of incident spinal
fracture in a complete population. Spine 21:492–499, 1996
23. Inaba K, Kirkpatrick AW, Finkelstein J, et al: Blunt abdominal
aortic trauma in association with thoracolumbar spine fractures.
Injury 32:201–207, 2001
24. Kaneda K, Abumi K, Fujiya M: Burst fractures with neurolog-
ic deficits of the thoracolumbar-lumbar spine. Results of ante-
rior decompression and stabilization with anterior instrumenta-
tion. Spine 9:788–795, 1984
25. Karnaze MG, Gado MH, Sartor KJ, et al: Comparison of MR
and CT myelography in imaging the cervical and thoracic
spine. AJR 150:397–403, 1988
26. Keenen TL, Anthony J, Benson DR: Dural tears associated with
lumbar burst fractures. J Orthop Trauma 4:243–245, 1990
27. Kostuik JP, Harrington I, Alexander D, et al: Cauda equina syn-
drome and lumbar disc herniation. J Bone Joint Surg 68:
386–391, 1986
28. Laasonen EM, Kivioja A: Delayed diagnosis of extremity
injuries in patients with multiple injuries. J Trauma 31:
257–260, 1991
29. Malas MA, Salbacak A, Buyukmumcu M, et al: An investiga-
tion of the conus medullaris termination level during the period
of fetal development to adulthood. Kaibogaku Zasshi 76:
453–459, 2001
30. McCormick PC: Retropleural approach to the thoracic and tho-
racolumbar spine. Neurosurgery 37:908–914, 1995
31. Miller CA, Dewey RC, Hunt WE: Impaction fracture of the
lumbar vertebrae with dural tear. J Neurosurg 53:765–771,
1980
32. Miller CA, Hunt WE: Variation of impaction fracture of the
lumbar spine. J Neurosurg 56:603, 1982
33. Mixter WJ, Barr JS: Rupture of the intervertebral disc with
involvement of the spinal canal. N Engl J Med 211:210–215,
1934
34. Morgan TH, Wharton GW, Austin GN: The results of laminec-
tomy in patients with incomplete spinal cord injuries. Para-
plegia 9:14–23, 1971
35. Pick TP, Howden R (eds): Anatomy, Descriptive and Surg-
ical. By Henry Gray. New York: Bounty Books, 1977
36. Rabinovici R, Ovadia P, Mathiak G, et al: Abdominal injuries
associated with lumbar spine fractures in blunt trauma. Injury
30:471–474, 1999
37. Schaefer DM, Flanders A, Northrup BE, et al: Magnetic reso-
nance imaging of acute cervical spine trauma. Correlation with
severity of neurologic injury. Spine 14:1090–1095, 1989
38. Silvestro C, Francaviglia N, Bragazzi R, et al: On the predictive
value of radiological signs for the presence of dural lacerations
related to fractures of the lower thoracic or lumbar spine. J
Spinal Disord 4:49–53, 1991
39. Singer KP, Jones TJ, Breidahl PD: A Comparison of radio-
graphic and computer-assisted measurements of thoracic and
thoracolumbar sagittal curvature. Skeletal Radiol 19:21–26,
1990
40. Tekkok IH, Carter DA, Brinker R: Spinal subdural haematoma
as a complication of immediate epidural blood patch. Can J
Anaesth 43:306–309, 1996
41. Vapalahti M, Kuurne T: Acute paraplegia caused by a sponta-
neous extradural haematoma of the conus medullaris area. Acta
Chir Scand 141:484–487, 1975
Manuscript received December 29, 2004.
Accepted in final form May 17, 2004.
Address reprint requests to: James Harrop, M.D., 909 Walnut
Street, Third Floor, Philadelphia, Pennsylvania 19107. email:
James.Harrop@jefferson.edu.
23